Based on the follow-up investigation made on the employment of university graduates in pharmacy,we analyzed the situation of their jobs,salary and their attitude towards pharmacy and suggested some mothods to promote the graduates employment and give the students the career guidance.Up to now,492 students have graduated,the first employment rate was 78%,and last employment rate was 100%.

Ex-RAD (ON01210) is a novel and efficient anti-radiation drug with low toxicity developed by US army and Onconova Pharmaceuticals in recent years. The significant survival advantage and low toxicity of Ex-RAD have contributed to the approval by the FDA as an investigational new drug in December 2008. Meanwhile, the drug is currently in phase I clinical trials in humans. In this paper, the chemical structure, synthesis route, detection method and pharmacological action of Ex-RAD were reviewed, and the appli-cation prospect of Ex-RAD was also explored.

The most toxic DNA damage is DNA double strand breaks (DSBs), which are mainly repaired by non-homologous end joining (NHEJ). DNA-dependent protein kinase (DNA-PK) belongs to phosphatidylinositol-3-kinase-related protein kinase family (PIKK) and plays a key role in NHEJ. DNA-PK is overexpressed in a variety of cancer cells and is related to the occurrence, development and drug resistance of malignant tumors. In this article, the representative DNA-PK inhibitors with anticancer effects are reviewed, in order to provide a reference to discovery novel DNA-PK inhibitors.

Background Posterior capsular opacification(PCO) is common complication after extrecapsular extract of cataract.Matrix metalloproteinases-3 (MMP-3) can degrade all the extracellular matrix except polyose.The gene therapy of PCO upon MMP-3 is the researching hot topic.Fibronectin ( FN ) is a degrade gelatin,so its expression can reflect the effect of MMP-3 on LECs indirectly. Objective The aim of this study was to construct MMP-3 eukaryotic recombination plasmid and transfect to lens epithelium cells(LECs) for the observation of MMP3 expression,and to explore the feasibility of gene therapy for after cataract. Methods Six fresh lenses were obtained from pigs.LECs were cultured using explant method.The eukaryotic expression vector pEGFP-N1-MMP-3 was reconstructed with MMP-3 and pEGFP-N1 plasmids.The accuracy of MMP-3 gene fragment was confirmed by double enzyme digestion and DNA sequencing analysis.After transfecting pEGFP-N1-MMP-3 into LECs of pig,the expression of MMP-3 protein in the cells was indirectly observed by green fluorescent protein.The expression of FN in LECs was detected using Western blot. Results The result of double enzyme digestion was consistent with the base number of pEGFP-N1 plasmids and target fragment.By enlacing the result of DNA sequencing analysis with software,the resemblance of the DNA sequence of MMP-3 from recombination plasmid pEGFP-N1-MMP-3 and that of homo MMP-3 was 99.6％,indicating that the target fragment was inserted to pEGFP-N1 plasmids successfully.Green fluorescence for GFP was seen in the LECs in pEGFP-N1-MMP-3 transfected group,but absent response for GFP was in empty vector group.Western blot revealed that the relative expression level of FN in LECs was 0.666±0.008 in pEGFP-N1-MMP-3 trasfected group and 0.326 ±0.071 in empty vector group,with a significant difference between these two groups(P=0.000). Conclusions Eukaryotic recombination plasmid pEGFP-N1-MMP-3 is successfully constructed,and MMP-3 can be expressed in LECs after transfected.These results lay a foundation for the further research of MMP-3 gene therapy for PCO.

Animals ; Bone and Bones ; metabolism ; Energy Metabolism ; physiology ; Humans ; Osteocalcin ; metabolism

Background Human paired box gene 6 (PAX6)encodes a transcriptional regulator.It is essential for eye and brain morphogenesis.Mutation of PAX6 gene isresponsible for many congenital ocular malformations,such as aniridia.Aniridia is a autosomal dominant inheritance mode.Objective In this study,PAX6 gene mutation was analyzed in three Chinese families with aniridia through polymerase chain reaction (PCR) and sequencing.Methods The blood specimens were collected from 5 suffers and normal individuals of 3 aniridia families to extract DNA.The sequences of extron 4-13 were designed based on PAX6 gene.The primer was amplified by PCR and sequenced and compared with the known PAX6 gene sequence.This study complied with Declaration of Helsinki and approved by ethic committee of Sichuan University.Written informed consent was obtained from each individual before any medial examination.ResultsThere were 5 suffers in the 3 families.A heterozygous mutation (c.718 C＞T) in PAX6 gene was identified in 2 patients of family A.This mutation caused an amino acid substitution of arginine to termination codon at position 240 ( p.Arg240X) of PAX6 protein.No similar change in the normal families.No any the alteration of PAX6 gene was detected in family B whatever suffers and normal individuals.In family C,a deletion mutation of c.331 delG ( p.Val111 SerfsX13 ) in PAX6 gene was found.The deletion of one base caused frame shift mutation of PAX6 protein,and no such mutation was seen in other families.Conclusions Mutation of PAX6 gene appeares to be causative mutations of the disease in family A and C.

OBJECTIVETo screen the mutation of the beta and gamma subunits of epithelial sodium channel gene SCNN1 in two families with Liddle's syndrome.

METHODSTwo patients clinically diagnosed as Liddle's syndrome and their family members were enrolled. Peripheral blood samples were collected and total genomic DNA was prepared. Polymerase chain reaction (PCR) was used to amplify the exon 13 of the SCNN1B and SCNN1G gene. PCR products were purified and subjected to direct DNA sequencing.

RESULTSA heterozygous nonsense mutation at codon 564 of the SCNN1B gene from CGA(Arg) to stop codon(TGA) was detector in the proband of family 1. More importantly, a novel heterozygous nonsense mutation of CAG(Gln) to stop codon TAG at codon 567 of the SCNN1G gene was detected in the proband and another two members of family 2.

CONCLUSIONScreening for specific mutations of the SCNN1 gene in relatives of patients with Liddle's syndrome can be used to identify the previously unrecognized cases within the family. A new nonsense mutation(Q567X) of the SCNN1G gene is likely the cause of Liddle's syndrome in family 2.

Adult ; Asian Continental Ancestry Group ; genetics ; Base Sequence ; Case-Control Studies ; DNA Mutational Analysis ; Epithelial Sodium Channels ; genetics ; Female ; Humans ; Liddle Syndrome ; genetics ; Male ; Mutation ; genetics ; Pedigree ; Young Adult

Objective This study was operated to investigate the association between urinary albumin-to-creatinine ratio (UACR) and physical situations as hypertension and prehypertension among women.Methods Blood pressure,height,weight and waist circumference were measured and factors such as cigarette smoking,alcohol intake,family history of hypertension,were investigated.Blood glucose and lipid,serum uric acid,urinary albumin and urinary creatinine were tested on 1796 women aged ≥30 years living in the Jinchang district of Suzhou.Associations between UACR and hypertension as well as prehypertension were analyzed,by using ordinal multinomial logistic regression models.Results The mean levels of UACR were 15.54 (7.67,32.53),9.01 ( 5.45,18.06),7.13 (4.60,12.50 ) mg/g and the rates of higher UACR were 27.57％,13.42％,9.61％ in hypertensive,pre-hypertensive and normotensive subjects,respectively,with significant differences noticed among the three groups (P＜0.05).The average systolic blood pressure/diastolic blood pressure appeared to be 125.3/80.9,128.8/82.7,130.8/84.0 and 135.1/85.9 mm Hg for participants with UACR in the first,second,third and fourth quartile,respectively.The risks of prehypertension or hypertension increased with increasing UACR levels.Dose-response relationship was seen between UACR and risks of prehypertension or hypertension.Multivariable adjusted odds ratios (95％CI) of prehypertension or hypertension in the upper quartiles of UACR were 1.32 ( 1.02,1.70),1.72 ( 1.32,2.24),and 2.37 (1.80,3.11 ),respectively,when compared with the lowest quartile.Conclusion Elevated UACR was associated with both hypertension and prehypertension among women.

BACKGROUNDRheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disorder. Many methods have been used to observe the progress of RA. The purpose of this study was to observe the progress of RA in rats with 18F-fluorodeoxyglucose (FDG) positron emission tomography/computed tomography (PET/CT), magnetic resonance (MR) imaging and arthritis score, and analyze the relationships among different methods in evaluation of RA.

METHODSSixteen healthy Sprague Dawley (SD) rats about 8-week old were randomly assigned to a RA group and a control group. Bovine type II emulsified incomplete Freud's adjuvant was used to induce arthritis in the RA group. Arthritis score of the rats in two groups were recorded, and (18)F-FDG PET/CT, MR imaging were performed both on the corresponding rats every 3 days. All the rats were sacrificed at week 5, and histopathological examination was performed on rat knees stained with haematoxylin and eosin.

RESULTSThe arthritis score and the standard uptake value (SUV) of knee joints in RA rats increased with the progression of arthritis gradually. Both peaks of arthritis score and SUV appeared at 21 days after the first immune injection, then the arthritis score and SUV of knee joints decreased slowly. The arthritis scores of knee joints in RA rats were positively correlated with their SUV changes. The MR images were confirmed by the histopathological studies.

CONCLUSIONPET/CT can detect the earliest molecular metabolism changes of RA, and MR imaging can follow up the dynamical anatomical changes of RA, all of which indicated that PET/CT and MR imaging may be applied as useful tools to monitor the progress of RA.

Animals ; Arthritis, Rheumatoid ; diagnosis ; pathology ; Fluorodeoxyglucose F18 ; Magnetic Resonance Imaging ; Positron-Emission Tomography ; Radiopharmaceuticals ; Rats ; Rats, Sprague-Dawley ; Tomography, X-Ray Computed

OBJECTIVETo explore the blockade effect of phenylbutyrate (PB), a histone deacetylase inhibitor, on the in vitro biological function of AML1/ETO to reverse its transcription repression and induce Kasumi-1 cells to differentiate and apoptosis.

METHODSKasumi-1 cells were treated with PB at different concentrations in suspension culture. Cell proliferation was analysed by MTT assay, morphological changes by light and electron microscopy, expression of myeloid-specific differentiation antigen and cell cycle by flow cytometry, cell apoptosis by annexin V staining, agarose gel electrophoresis and flow cytometry.

RESULTSPB treatment caused a dose-dependent inhibition of the cell proliferation. The IC(50) was about 2.3 mmol/L. PB treatment led to a progressive decline in the fraction of S-phase cells and increase in G(0)/G(1) cells. PB induced a time- and dose-dependent increase in expression of myeloid cell surface protein CD(11b) and CD(13). A dose-dependent increase in early apoptosis for 2 days treatment, late apoptosis for 3 days treatment. The DNA ladder of apoptosis was observed on agarose gel electrophoresis for 5 days treatment. Morphological features of monocytoid differentiation and apoptosis were seen on Wright-Giemsa staining smears.

CONCLUSIONPB treatment could inhibit proliferation of Kasumi-1 cells, induce partial differentiation, apoptosis and accumulation of cells in G(0)/G(1) phase.

Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cell Division ; drug effects ; Cell Line, Tumor ; Dose-Response Relationship, Drug ; Histone Deacetylase Inhibitors ; Humans ; Leukemia, Myeloid, Acute ; pathology ; Phenylbutyrates ; pharmacology